Elevated ventricular filling pressures ultimately result in systemic and pulmonary venous congestion and edema, and are thus largely responsible for the manifestations of congestive heart failure. The goal of this research proposal is to assess the role of incomplete relaxation and ventricular visco-elastic properties in the development of elevated ventricular filling pressures. Recent studies have shown a shift in the left ventricular diastolic pressure volume relationship during angina pectoris such that there is a higher diastolic pressure at any given chamber volume. Current studies are attempting to elucidate th mechanism for this phenomenon.